title: Obese mice are resistant to eosinophilic airway inflammation induced by diesel exhaust particles.
abstract: Particulate matter can exacerbate respiratory diseases such as asthma. Diesel exhaust particles are the substantial portion of ambient particulate matter with a <2.5 µm diameter in urban areas. Epidemiological data indicate increased respiratory health effects of particulate matter in obese individuals; however, the association between obesity and diesel exhaust particle-induced airway inflammation remains unclear. We aimed to investigate the differences in susceptibility to airway inflammation induced by exposure to diesel exhaust particles between obese mice (db/db) and lean mice (db/+m). Female db/db and db/+m mice were intratracheally administered diesel exhaust particles or vehicle every 2 weeks for a total of seven times. The cellular profile of bronchoalveolar lavage fluid and histological changes in the lungs were assessed and the lungs and serum were analyzed for the generation of cytokines, chemokines and soluble intercellular adhesion molecule 1. Diesel exhaust particle exposure-induced eosinophilic infiltration in db/+m mice accompanied by T-helper 2 cytokine, chemokine and soluble intercellular adhesion molecule 1 expression in the lungs. In contrast, it induced mild neutrophilic airway inflammation accompanied by elevated cytokines and chemokines in db/db mice. The lungs of db/db mice exhibited decreased expression of eosinophil activators/chemoattractants such as interleukin-5, interleukin-13 and eotaxin compared with those of db/+m mice. In addition, serum eotaxin and monocyte chemotactic protein-1 levels were significantly higher in db/db mice than in db/+m mice. In conclusion, obesity can affect susceptibility to diesel exhaust particle-induced airway inflammation, which is possibly due to differences in local and systemic inflammatory responses between lean and obese individuals.
authors.affiliation: Center for Environmental Health Sciences, National Institute for Environmental Studies, 16-2 Onogawa, Tsukuba, 305-8506, Japan.
authors.forename: Rie
authors.initials: R
authors.lastname: Yanagisawa
authors.forename: Eiko
authors.initials: E
authors.lastname: Koike
authors.forename: Takamichi
authors.initials: T
authors.lastname: Ichinose
authors.forename: Hirohisa
authors.initials: H
authors.lastname: Takano
mesh_terms: D000818:Animals; D001992:Bronchoalveolar Lavage Fluid / Q000276:immunology; D018925:Chemokines / Q000097:blood; D002634:Chemotaxis, Leukocyte; D016207:Cytokines / Q000097:blood; D004195:Disease Models, Animal; D005260:Female; D018799:Intercellular Adhesion Molecule-1 / Q000097:blood; D008168:Lung / Q000187:drug effects* / Q000276:immunology / Q000473:pathology; D008820:Mice, Obese; D009504:Neutrophils / Q000187:drug effects / Q000276:immunology; D009765:Obesity / Q000097:blood / Q000276:immunology*; D052638:Particulate Matter / Q000633:toxicity*; D011657:Pulmonary Eosinophilia / Q000097:blood / Q000139:chemically induced / Q000276:immunology / Q000473:pathology / Q000517:prevention & control*; D001335:Vehicle Emissions / Q000633:toxicity*
chemical_list: D018925:Chemokines; D016207:Cytokines; C090509:Icam1 protein, mouse; D052638:Particulate Matter; D001335:Vehicle Emissions; D018799:Intercellular Adhesion Molecule-1
keywords: airway inflammation; chemokines; cytokines; diesel exhaust particles; eosinophil; neutrophil